Gabpα-Pparγ Complex Determines Glycolytic Capacity and Lactic Acid Homeostasis in Brown Fat
Wang Z., Wang H., Kang Q., Pan R., He R., Yang M.
Animal Study, published in Adv Sci (Weinh) (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Adv Sci (Weinh) (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41276932
- PMCID
- PMC12884720
- DOI
- 10.1002/advs.202517426
- Citations
- 1
Abstract (original English)
Glycolysis in brown adipose tissue (BAT) plays a critical role in fueling thermogenesis. However, the transcriptional control of glycolysis in brown fat remains poorly understood. Here, GA binding protein alpha chain (Gabpα) is identified as a key transcriptional regulator that sustains the glycolytic capacity of brown adipocytes. Gabpα is preferentially expressed in BAT, yet BAT-specific ablation of Gabpα substantially impairs glycolytic flux and heat production, leading to reduced glucose tolerance and impaired cold tolerance. Mechanistically, the C-terminus of the Gabpα protein directly interacts with peroxisome proliferator-activated receptor-γ (Pparγ) and synergistically promotes transcription of the glycolytic gene enolase 1 (Eno1). Disruption of the Gabpα-Pparγ interaction in BAT significantly suppresses glycolysis, reduces energy expenditure, and induces cold intolerance in mice. Notably, inhibition of Gabpα-Pparγ binding also decreases lactic acid concentration and downregulates lactate dehydrogenase (Ldh) expression, resulting in the suppression of uncoupling protein 1 (Ucp1) expression and thermogenesis. Conversely, adipose-specific overexpression of Gabpα markedly enhances BAT glycolytic and thermogenic activity, protecting against cold challenge and high-fat diet (HFD)-induced obesity. Collectively, these results point to the Gabpα-Pparγ complex as a potent regulat
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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